The sources of vitamin D

Humans obtain vitamin Dfrom dietary sources and supplements, but mainly from sunlight exposure1, 2. Most natural foods contain only small amounts of this fat-soluble vitaminand these quantities are generally inadequate to maintain vitamin D sufficiency. Consequently, the dietary content of vitamin D is usually insufficient to maintain an adequate vitamin D status and cutaneous (skin) synthesis of vitamin D3 on exposure to UVB radiation is essential for vitamin D adequacy, unless fortified foods are eaten or supplements are used3. Thus, if there is insufficient UVB sunlight exposure for adequate cutaneous synthesis of vitamin D, it becomes an essential nutrient4.

Dietary sources of vitamin D include fatty fish, some fish liver oils, organ meats, egg yolks and also fortified foods5, for example certain margarines in South Africa. In Africa, data on dietary vitamin D intake are scarce6. From the little available data on food patterns and sources of intakes of other nutrients, the contribution of dietary sources to vitamin D intake does not seem to be substantial on this continent6. This is primarily because few naturally occurring food sources are rich in vitamin D and in many areas these foods are consumed infrequently or not at all7-9.

Vitamin D obtained from sun exposure, food and supplements is biologically inert and must undergo two hydroxylations in the body for activation. The first occurs in the liver where 25-hydroxyvitamin D (25(OH)D), also known as calcidiol, is formed. The second occurs primarily in the kidney and forms the physiologically active 1,25-dihydroxyvitamin D [1,25(OH)2D], also known as calcitriol.

Vitamin D from sun exposure

Solar ultraviolet B (UVB) radiation enters the skin and converts a substance in the skin, called 7-dehydrocholesterol (7-DHC), to previtamin D3, which swiftly converts to vitamin D3 (cholecalciferol), one of the main forms of vitamin D. Excessive solar exposure does not result in vitamin D3 toxicity, as any excess previtamin D3 or vitamin D3 is destroyed by solar exposure10.

Any interference with the penetration of UVB sunlight into the skin and anything that reduces the transmission of UVB sunlight to the surface of the earth will influence the cutaneous synthesis of vitamin D311, 12. Therefore, even with plentiful sunshine, the degree of UVB skin exposure also depends on living and working environments and clothing13 and diets poor in vitamin D can compound risk for vitamin D insufficiency. Sunscreen absorbs UVB radiation and topical application of a factor 15 sunscreen has been shown to absorb 99% of UVB sunlight14. Increased skin pigmentation distinctly decreases vitamin D3 synthesis as eumelanin pigment in the skin competes with 7-DHC for UVB photons and slows the rate of conversion to previtamin D3. People with darker skin require a longer period of time to make sufficient pre-vitamin D315, 16.

Season, latitude and time of day also impact cutaneous vitamin D3 synthesis. The quantity of UVB photons that reach the earth’s surface is affected by the angle at which sun strikes the earth. Only small amounts, if any, vitamin D3 synthesis occurs during winter, early morning and late afternoon, when the zenith angle is increased12, 17. Little or no vitamin D3 can be produced at latitudes above approximately 30 degrees north and south during winter months12. For example, in the southern hemisphere, people living in Buenos Aires (Argentina) and Cape Town (South Africa), can make far less vitamin D from the sun during winter months (June through August) than they can during their spring and summer. In the northern hemisphere, residents in Boston (USA), Edmonton (Canada), and Bergen (Norway) are not able to make enough vitamin D from the sun for 4, 5, and 6 months of the year18.The body stores vitamin D from sun exposure during the summer, but stores must last for many months and by late winter, many people living in these higher-latitude areas are deficient10.

Vitamin D: functions and role in health

The principal physiologic function of vitamin D in humans is to maintain intracellular and extracellular calcium homeostasis in order to ensure its availability for essential functions in bone and dental health. This is achieved through the action of 1,25(OH)2D, the biologically active form of vitamin D, which regulates calcium and phosphorus metabolism in the bone and intestine5, 19. In addition to these well-known effects, more recent research has demonstrated that vitamin D exerts its influence on many physiologic processes. These include modulation of cell growth, neuromuscular and immune function, and reduction of inflammation. Many genes encoding proteins that regulate cell proliferation, differentiation, and apoptosis are modulated in part by vitamin D. Many cells have vitamin D receptors and some convert 25(OH)D to 1,25(OH)2D20. Vitamin D has been associated with a variety of health risks and conditions, including type 1 and type 2 diabetes, hypertension, glucose intolerance and multiple sclerosis20. However, most evidence for the roles of vitamin D in these diseases comes from in vitro, animal and observational studies. Before vitamin D can be recommended as an adjunctive therapy for the treatment or prevention of these diseases, evidence from more rigorously designed clinical trials is needed.

How much vitamin D do we need?

The relative contributions of dietary sources and cutaneous synthesis exposure to UVB sunlight to vitamin D status are still uncertain and this has made it challenging for scientific authorities to establish dietary vitamin D requirements4. It is thus not surprising that a range of authoritative dietary guidelines for vitamin D for specific age groups have been formulated and there is considerable variation in these recommendations21-23.

Very recently, the US DRIs committee for calcium and vitamin D of the Food and Nutrition Board of the Institute of Medicine set an Estimated Average Requirement (EAR) of 10 micrograms (µg) (400 International Units [IU]) and a Recommended Dietary Allowance (RDA) of 15 µg (600 IU) for vitamin D for adults 19 to 70 years20. The previous DRIs for vitamin D included only an Adequate Intake (AI) and Tolerable Upper Intake Level (UL)24. For the establishment of the new recommendations, the DRI committee used evidence of serum25 (OH)D levels that benefited bone health, such as maximising calcium absorption, positive outcomes on bone mineral content and prevention of rickets. However, the committee pointed out that the confounding effect of sunlight exposure has not yet been addressed adequately and advised that it would be ideal if the relative contribution made by sunlight exposure to overall serum 25(OH)D levels could be quantified in formulating the EAR. The committee did, however propose that due to the public health concerns related to sun exposure and skin cancer risk, vitamin D requirements cannot be based on a “recommended” or conventional level of sun exposure20. As is, the committee in establishing the recent EAR and RDA for vitamin D, followed an approach that focused on identifying the vitamin D intakes that will maintain serum 25 (OH)D levels above selected cut-offs when cutaneous synthesis is considerably reduced or absent20.

Measuring vitamin D status

Serum 25-hydroxyvitamin D (25(OH)D) levels is regarded as the best measure of vitamin D status in humans25, 26. While vitamin D deficiency is commonly defined as a 25(OH)D level of less than or equal to 20 nanograms per millilitre (ng/mL), other cut-offs have been used to define vitamin D status and there has been much debate in the literature about optimal serum 25(OH)D levels for the attainment and maintenance of bone mass10, 27, 28. In view of current data, there is some agreement that in adults, vitamin D deficiency is a circulating 25(OH)D concentration of less than 20 ng/mL and vitamin D insufficiency is a 25(OH)D concentration of 20 to 29 ng/mL. Concentrations of 30 ng/ mL and above are considered sufficient10, 12, 29. This is based on data showing that intestinal calcium absorption is maximal above 32 ng/mL30 and that parathyroid hormone levels in adults carry on declining and reach their nadir at between 30 and 40 ng/mL31-33. Other researchers have reported 25(OH)D levels of 32 ng/mL and above as being sufficient34, 35.

Global vitamin D status

Vitamin D deficiency has been found to be widespread in certain subpopulations (using various cut-off points), even among those living in countries with abundant sunshine36, 37. A recent systematic review of the worldwide literature provided a graphical illustration of global vitamin D status38. Areas where data on vitamin D status was lacking included Central America, South America (with the exception of Brazil) and much of Africa. Among adults it was found that in most regions that offer some data, levels of 25(OH)D varied from between 10 and 20 ng/mL and between 20 and 30 ng/mL.

In Africa, seasonal effects on cutaneous synthesis of vitamin D3 would be expected in countries that are located at latitudes greater than 30 degrees north and south, such as South Africa, Egypt, Morocco, Libya, Tunisia and Algeria6. South Africa, especially the country’s southern coast, has a highly seasonal pattern of UVB exposure which affects the potential for cutaneous vitamin D production. An earlier study in Cape Town found only limited vitamin D synthesis in vitro in the winter months from April through to September39. Further studies are investigating vitamin D status and potential impacts of vitamin D nutriture on health outcomes in the southern areas of South Africa40, 41, specifically in relation to infectious diseases.